Boosting Self-Repair May Preserve Brain in Alzheimers and Parkinsons

In Alzheimer’s, Parkinson’s, variant Creutzfeldt-Jakob and other brain-wasting prion diseases, cells in the brain gradually deteriorate, begin to function abnormally, and die. However, some parts of the brain have the capacity to self-repair and make new brain cells. A new study suggests there could be a way to harness this and perhaps preserve brain function in neurodegenerative diseases.

Writing in the journal Brain, study leader Dr. Diego Gomez-Nicola and colleagues from the Centre for Biological Sciences at the University of Southampton in the UK describe how previous studies have already revealed that even in neurodegenerative diseases there is evidence that the brain carries on attempting to repair itself.

One area of the brain that shows evidence of self-repair or neurogenesis is the dentate gyrus, which forms part of the hippocampus, which controls learning and memory.

Studying the brains of mice with a prion disease, the team found evidence of increased self-repair in the dentate gyrus that partially compensated for the loss of brain cells caused by the disease.

Their detailed investigation helped them identify how the new brain cell populations were generated over time, and how they integrated with existing brain circuits.

They found that as long as the self-repair occurred in the early or middle stages of the brain-wasting disease, new brain cells integrated into existing circuits in a way that preserved some brain function – but this failed when the disease was advanced.

Postmortem samples also suggest evidence of self-repair in diseased human brain The team says they also found evidence to suggest increased self-repair in postmortem brain samples of patients who had variant Creutzfeldt-Jakob disease and Alzheimer’s disease when they died.

The authors conclude that the brain has some ability to orchestrate self-repair and suggest there is a time-limited window of opportunity for potential treatments to boost this mechanism and preserve brain function in patients with neurodegenerative diseases. Gomez-Nicola says the study opens new avenues “to identify what specific signals are used to promote this increased neurogenic response, with views focused in targeting neurogenesis as a therapeutic approach to promote the regeneration of lost neurons.” As they strike primarily in mid- to late-life, neurodegenerative diseases become increasingly more common in aging populations. For instance, in the US, where estimates suggest by 2030 around 20% of the population will be over the age of 65, some 5 million Americans are living with Alzheimer’s disease and another 1 million have Parkinson’s. Finding treatments and cures for neurodegenerative diseases has never been more urgent. Funds from the European Union Seventh Framework Programme and the Medical Research Council helped finance the study.

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